Date of Award


Document Type

Honors Thesis

Degree Name

Bachelor of Science



Advisor/Committee Chair

Cara T. Pager


Currently over 180 million people are infected with Hepatitis C virus (HCV) worldwide. HCV infection is a major cause of hepatocellular carcinoma (HCC), liver cirrhosis, and chronic hepatitis. The available antiviral treatment of interferon and ribavirin has limited success, is costly and toxic. Furthermore, there is no vaccine. An increased understanding of how HCV exploits the many cellular pathways and host factors during infection will provide information necessary for the development of novel anti-HCV therapies, which target host proteins rather than the rapidly evolving viral proteins. During infection, HCV interacts with and manipulates many host mRNA pathways. The Pager lab discovered that RCK, a DEAD-box helicase involved in microRNA gene regulation and mRNA decay, is required for HCV gene expression and virus assembly. RCK contains conserved motifs common to all DEAD-box helicases, as well as an extended N-terminus that contains a 48 amino acid prion-related domain mostly composed of glutamine and glycine residues. I hypothesize that the prion-related domain (PRD) facilitates the localization and function of RCK at HCV assembly sites. To test this hypothesis I used deletion analysis of the PRD to examine the effect of this deletion on RCK protein expression and localization and on HCV gene expression. This study will increase our understanding of HCV infection, as well as the normal cellular role of RCK.

Included in

Biology Commons